Journal article
DNA Variation in the SNAP25 Gene Confers Risk to ADHD and Is Associated with Reduced Expression in Prefrontal Cortex
Z Hawi, N Matthews, J Wagner, RH Wallace, TJ Butler, A Vance, L Kent, M Gill, MA Bellgrove
Plos One | PUBLIC LIBRARY SCIENCE | Published : 2013
Abstract
Background: The Coloboma mouse carries a ~2 cM deletion encompassing the SNAP25 gene and has a hyperactive phenotype similar to that of ADHD. Such mice are 3 fold more active compared to their control littermates. Genetic association studies support a role for allelic variants of the human SNAP25 gene in predisposing to ADHD. Methods/Principal Findings: We performed association analysis across the SNAP25 gene in 1,107 individuals (339 ADHD trios). To assess the functional relevance of the SNAP25-ADHD associated allele, we performed quantitative PCR on post-mortem tissue derived from the inferior frontal gyrus of 89 unaffected adults. Significant associations with the A allele of SNP rs362990..
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Awarded by National Institutes of Health
Funding Acknowledgements
ZH and MAB were supported by the Australian National Health and Medical Research council (NHMRC) grants APP1002458 and MAB, AV and RHW (569636). MAB is supported by an NHMRC Career Development Award (569631). The funders had no role in study design, data collection, and analysis, decision to publish, or operation of the manuscript. The authors would like to acknowledge the support of participating families. We would also like to acknowledge the Queensland Brain Bank and the Victorian Brain Bank for providing the non-pathological brain tissue samples. These centers are funded by the Australia's National Health and Medical Research council (NHMRC). Tissues were also obtained from the New South Wales Tissue Resource Centre at the University of Sydney which is supported by the National Health and Medical Research Council of Australia, Schizophrenia Research Institute, National Institute of Alcohol Abuse and Alcoholism (NIH (NIAAA) R24AA012725.